Laser aggregometer studies, ATP release and thromboxane B2 release and cAMP concentration of the platelets in nephrotic syndrome

S. Túri, C. Bereczki, Cs Torday, Z. Havass

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Abstract

Platelet function was studied in 56 children with nephrotic syndrome, 33 were on oral prednisolone (P) treatment (group 1), while 23 were in early (<6 months) remission (group 2): 12 on P (group 2a) and 11 not on P (group 2b), and there were 18 controls (group 3). The following tests were used: platelet aggregation with collagen in a laser rheoaggregometer; adenosine triphosphate (ATP) release: during aggregation with luciferin-luciferase in a lumiaggregometer; thromboxane B2 (TXB2) release: by radio-immunoassay; platelet cAMP concentration: by binding assay. The changes in plasma cholesterol (C) and triglycerides (TG) were compared with the platelet aggregation results. Patients in group 1 and 2 exhibited significantly higher aggregability, TXB2 release and ATP release in response to collagen than those in group 3 (p <0.01), but there was no difference between groups 1 and 2 or groups 2a and 2b. Some differences were observed between the histological groups. Patients with IgA and SLE nephropathy displayed higher aggregability than those with minimal change nephrotic syndrome in remission (p <0.05). The highest level was in membranous nephropathy. The platelet cyclic adenosine monophosphate (cAMP) concentration was significantly lower in groups 1 and 2 than in group 3 (p <0.001). No differences were observed between groups 1 and 2 or between groups 2a and 2b. Plasma C and TG levels did not show any correlation with the platelet aggregation. The increased platelet aggregation, TXB2 release and ATP release and decreased cAMP concentration in the platelets may play a role in the pathogenesis of nephrotic syndrome which remains altered in early remission. Oral P and plasma lipids did not change the platelet function significantly.

Original languageEnglish
Pages (from-to)69-73
Number of pages5
JournalProstaglandins Leukotrienes and Essential Fatty Acids
Volume51
Issue number1
DOIs
Publication statusPublished - 1994

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Thromboxane B2
Nephrotic Syndrome
Platelets
Cyclic AMP
Lasers
Platelet Aggregation
Blood Platelets
Adenosine Triphosphate
Agglomeration
Triglycerides
Collagen
Lipoid Nephrosis
Membranous Glomerulonephritis
Plasmas
Prednisolone
Luciferases
Radio
Immunoassay
Immunoglobulin A
Cholesterol

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

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title = "Laser aggregometer studies, ATP release and thromboxane B2 release and cAMP concentration of the platelets in nephrotic syndrome",
abstract = "Platelet function was studied in 56 children with nephrotic syndrome, 33 were on oral prednisolone (P) treatment (group 1), while 23 were in early (<6 months) remission (group 2): 12 on P (group 2a) and 11 not on P (group 2b), and there were 18 controls (group 3). The following tests were used: platelet aggregation with collagen in a laser rheoaggregometer; adenosine triphosphate (ATP) release: during aggregation with luciferin-luciferase in a lumiaggregometer; thromboxane B2 (TXB2) release: by radio-immunoassay; platelet cAMP concentration: by binding assay. The changes in plasma cholesterol (C) and triglycerides (TG) were compared with the platelet aggregation results. Patients in group 1 and 2 exhibited significantly higher aggregability, TXB2 release and ATP release in response to collagen than those in group 3 (p <0.01), but there was no difference between groups 1 and 2 or groups 2a and 2b. Some differences were observed between the histological groups. Patients with IgA and SLE nephropathy displayed higher aggregability than those with minimal change nephrotic syndrome in remission (p <0.05). The highest level was in membranous nephropathy. The platelet cyclic adenosine monophosphate (cAMP) concentration was significantly lower in groups 1 and 2 than in group 3 (p <0.001). No differences were observed between groups 1 and 2 or between groups 2a and 2b. Plasma C and TG levels did not show any correlation with the platelet aggregation. The increased platelet aggregation, TXB2 release and ATP release and decreased cAMP concentration in the platelets may play a role in the pathogenesis of nephrotic syndrome which remains altered in early remission. Oral P and plasma lipids did not change the platelet function significantly.",
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AU - Bereczki, C.

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AU - Havass, Z.

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AB - Platelet function was studied in 56 children with nephrotic syndrome, 33 were on oral prednisolone (P) treatment (group 1), while 23 were in early (<6 months) remission (group 2): 12 on P (group 2a) and 11 not on P (group 2b), and there were 18 controls (group 3). The following tests were used: platelet aggregation with collagen in a laser rheoaggregometer; adenosine triphosphate (ATP) release: during aggregation with luciferin-luciferase in a lumiaggregometer; thromboxane B2 (TXB2) release: by radio-immunoassay; platelet cAMP concentration: by binding assay. The changes in plasma cholesterol (C) and triglycerides (TG) were compared with the platelet aggregation results. Patients in group 1 and 2 exhibited significantly higher aggregability, TXB2 release and ATP release in response to collagen than those in group 3 (p <0.01), but there was no difference between groups 1 and 2 or groups 2a and 2b. Some differences were observed between the histological groups. Patients with IgA and SLE nephropathy displayed higher aggregability than those with minimal change nephrotic syndrome in remission (p <0.05). The highest level was in membranous nephropathy. The platelet cyclic adenosine monophosphate (cAMP) concentration was significantly lower in groups 1 and 2 than in group 3 (p <0.001). No differences were observed between groups 1 and 2 or between groups 2a and 2b. Plasma C and TG levels did not show any correlation with the platelet aggregation. The increased platelet aggregation, TXB2 release and ATP release and decreased cAMP concentration in the platelets may play a role in the pathogenesis of nephrotic syndrome which remains altered in early remission. Oral P and plasma lipids did not change the platelet function significantly.

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